The development of the neuromuscular junction will be studied in vivo and in vitro utilizing cloned cell lines of nerve and muscle as well as organ culture techniques. The role of actin, basement membrane, energy and agonist in maintaining acetylcholine receptor at the sub-synaptic membrane will be investigated. Mutations that effect acetylcholine receptor expression will be isolated. The defect in myasthenia gravis will be investigated in order to determine the mechanism by which antibody stimulates acetylcholine receptor degradation. A mouse with a genetic defect which results in muscular dystrophy will be studied to determine why its acetylcholine receptor is degraded at a high rate. Monoclonal antibodies against antigens specific for the synapse will be produced.